ReviewJournal of cardiovascular pharmacology2017
Proinflammatory Cytokines Mediate GPCR Dysfunction.
Review in Journal of cardiovascular pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- An Explorative Approach to Examining the Role of Ischemia and Inflammation on the Function of Autoantibodies Against G Protein-Coupled Receptors and Their Corresponding Agonists.International journal of molecular sciences · 2026Article
- Vasopressor Strategy in Pediatric Sepsis: A Clinical Pharmacology Perspective.The journal of pediatric pharmacology and therapeutics : JPPT : the official journal of PPAG · 2026Article
- The Intricate Interplay of Noncoding RNAs and the Gut Microbiome in Gastrointestinal and Endocrine-Related Cancers.Sub-cellular biochemistry · 2026Review
- The Heart of the Matter: Immune Checkpoint Inhibitors and Immune-Related Adverse Events on the Cardiovascular System.Cancers · 2023Review
- Evaluation of qualitative and quantitative taste alterations in COVID-19.Biomolecules & biomedicine · 2023Observational
- Case Report: Neutralization of Autoantibodies Targeting G-Protein-Coupled Receptors Improves Capillary Impairment and Fatigue Symptoms After COVID-19 Infection.Frontiers in medicine · 2021Article
- Key Player in Cardiac Hypertrophy, Emphasizing the Role of Toll-Like Receptor 4.Frontiers in cardiovascular medicine · 2020Review
- Transcriptomic Validation of the Protective Effects of Aqueous Bark Extract ofFrontiers in pharmacology · 2019Article
- Tumor Necrosis Factor-α in Heart Failure: an Updated Review.Current cardiology reports · 2018Review
- Carvedilol Prevents Redox Inactivation of Cardiomyocyte ΒJACC. Basic to translational science · 2018Article
- Therapeutic Apheresis in Metabolic Syndrome.Immunology, endocrine & metabolic agents in medicinal chemistry · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Proinflammatory reaction by the body occurs acutely in response to injury that is considered primarily beneficial. However, sustained proinflammatory cytokines observed with chronic pathologies such as metabolic syndrome, cancer, and arthritis are detrimental and in many cases is a major cardiovascular risk factor. Proinflammatory cytokines such as interleukin-1, interleukin-6, and tumor necrosis factor α (TNFα) have long been implicated in cardiovascular risk and considered to be a major underlying cause for heart failure (HF). The failure of the anti-TNFα therapy for HF indicates our elusive understanding on the dichotomous role of proinflammatory cytokines on acutely beneficial effects versus long-term deleterious effects. Despite these well-described observations, less is known about the mechanistic underpinnings of proinflammatory cytokines especially TNFα in pathogenesis of HF. Increasing evidence suggests the existence of an active cross-talk between the TNFα receptor signaling and G-protein-coupled receptors such as β-adrenergic receptor (βAR). Given that βARs are the key regulators of cardiac function, the review will discuss the current state of understanding on the role of proinflammatory cytokine TNFα in regulating βAR function.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.